Evidence map›Paper›PMID 23129487›Full record

ArticleEMBO molecular medicine2012

WLS inhibits melanoma cell proliferation through the β-catenin signalling pathway and induces spontaneous metastasis.

Pei-Tzu Yang, Jamie N Anastas, Rachel A Toroni, Michi M Shinohara, Jamie M Goodson, Anja K Bosserhoff, Andy J Chien, Randall T Moon

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. G Protein-Coupled Receptor Signaling in Stem Cells and Cancer.International journal of molecular sciences · 2016
    Review
  10. Article
  11. Wls promotes the proliferation of breast cancer cells via Wnt signaling.Medical oncology (Northwood, London, England) · 2015
    Article
  12. Updating the Wnt pathways.Bioscience reports · 2014
    Article
  13. Article
  14. Review
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Pei-Tzu YangDepartment of Pharmacology, Howard Hughes Medical Institute, Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Jamie N Anastas
Rachel A Toroni
Michi M Shinohara
Jamie M Goodson
Anja K Bosserhoff
Andy J Chien
Randall T Moon
University of Washington · USHoward Hughes Medical Institute · USUniversity of Regensburg · DE

Funding

Self Renewal and Differentiation of Human Embryonic Stem CellsP01GM081619 · NIGMS · UNIVERSITY OF WASHINGTON · PI REH, THOMAS A · 2007 to 2017
$20.6M
Howard Hughes Medical InstituteNIGMS NIH HHS 5 P01 GM081619-04NIGMS NIH HHS P01 GM081619
6 · The paper itself

Abstract

Elevated levels of nuclear β-catenin are associated with higher rates of survival in patients with melanoma, raising questions as to how ß-catenin is regulated in this context. In the present study, we investigated the formal possibility that the secretion of WNT ligands that stabilize ß-catenin may be regulated in melanoma and thus contributes to differences in ß-catenin levels. We find that WLS, a conserved transmembrane protein necessary for WNT secretion, is decreased in both melanoma cell lines and in patient tumours relative to skin and to benign nevi. Unexpectedly, reducing endogenous WLS with shRNAs in human melanoma cell lines promotes spontaneous lung metastasis in xenografts in mice and promotes cell proliferation in vitro. Conversely, overexpression of WLS inhibits cell proliferation in vitro. Activating β-catenin downstream of WNT secretion blocks the increased cell migration and proliferation observed in the presence of WLS shRNAs, while inhibiting WNT signalling rescues the growth defects induced by excess WLS. These data suggest that WLS functions as a negative regulator of melanoma proliferation and spontaneous metastasis by activating WNT/β-catenin signalling.

Indexed as

Cell ProliferationSignal TransductionAnimalsbeta CateninCateninsCell Line, TumorCell MovementHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMelanomaMiceSkin NeoplasmsTransplantation, HeterologousWnt Proteinsbeta CateninCateninsIntracellular Signaling Peptides and ProteinsWnt Proteins

Identifiers

PMID23129487
PMCPMC3531604
OpenAlexW2148518190

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.